Search

Objective To test the association between recall for socially rewarding (positive) and/or socially critical (negative) information and depressive symptoms. Method Cohort study of people who had visited UK primary care in the past year reporting depressive symptoms ( N = 558, 69% female). Positive and negative recall was assessed at three time-points, 2 weeks apart, using a computerised task. Depressive symptoms were assessed at four time-points using the Beck Depression Inventory ( BDI). Analyses were conducted using multilevel models. Results Concurrently we found evidence that, for every increase in two positive words recalled, depressive symptoms reduced by 0.6 (95% CI −1.0 to −0.2) BDI points. This association was not affected by adjustment for confounders. There was no evidence of an association between negative recall and depressive symptoms (−0.1, 95% CI −0.5 to 0.3). Longitudinally, we found more evidence that positive recall was associated with reduced depressive symptoms than vice versa. Conclusion People with more severe depressive symptoms recall less positive information, even if their recall of negative information is unaltered. Clinicians could put more emphasis on encouraging patients to recall positive, socially rewarding information, rather than trying to change negative interpretations of events that have already occurred. [ABSTRACT FROM AUTHOR]

Objective: To test the association between recall for socially rewarding (positive) and/or socially critical (negative) information and depressive symptoms. Method: Cohort study of people who had visited UK primary care in the past year reporting depressive symptoms (N = 558, 69% female). Positive and negative recall was assessed at three time-points, 2 weeks apart, using a computerised task. Depressive symptoms were assessed at four time-points using the Beck Depression Inventory (BDI). Analyses were conducted using multilevel models. Results: Concurrently we found evidence that, for every increase in two positive words recalled, depressive symptoms reduced by 0.6 (95% CI -1.0 to -0.2) BDI points. This association was not affected by adjustment for confounders. There was no evidence of an association between negative recall and depressive symptoms (-0.1, 95% CI -0.5 to 0.3). Longitudinally, we found more evidence that positive recall was associated with reduced depressive symptoms than vice versa. Conclusion: People with more severe depressive symptoms recall less positive information, even if their recall of negative information is unaltered. Clinicians could put more emphasis on encouraging patients to recall positive, socially rewarding information, rather than trying to change negative interpretations of events that have already occurred. [ABSTRACT FROM AUTHOR]

BackgroundThe Beck Depression Inventory, 2nd edition (BDI-II) is widely used in research on depression. However, the minimal clinically important difference (MCID) is unknown. MCID can be estimated in several ways. Here we take a patient-centred approach, anchoring the change on the BDI-II to the patient's global report of improvement.MethodWe used data collected (n = 1039) from three randomized controlled trials for the management of depression. Improvement on a ‘global rating of change’ question was compared with changes in BDI-II scores using general linear modelling to explore baseline dependency, assessing whether MCID is best measured in absolute terms (i.e. difference) or as percent reduction in scores from baseline (i.e. ratio), and receiver operator characteristics (ROC) to estimate MCID according to the optimal threshold above which individuals report feeling ‘better’.ResultsImprovement in BDI-II scores associated with reporting feeling ‘better’ depended on initial depression severity, and statistical modelling indicated that MCID is best measured on a ratio scale as a percentage reduction of score. We estimated a MCID of a 17.5% reduction in scores from baseline from ROC analyses. The corresponding estimate for individuals with longer duration depression who had not responded to antidepressants was higher at 32%.ConclusionsMCID on the BDI-II is dependent on baseline severity, is best measured on a ratio scale, and the MCID for treatment-resistant depression is larger than that for more typical depression. This has important implications for clinical trials and practice. [ABSTRACT FROM PUBLISHER]

BackgroundAn argument often used to support the view that psychotic experiences (PEs) in general population samples are a valid phenotype for studying the aetiology of schizophrenia is that risk factors for schizophrenia show similar patterns of association with PEs. However, PEs often co-occur with depression, and no study has explicitly tested whether risk factors for schizophrenia are shared between PEs and depression, or are psychopathology specific, while jointly modelling both outcomes.MethodWe used data from 7030 subjects from a birth cohort study. Depression and PEs at age 18 years were assessed using self-report questionnaires and semi-structured interviews. We compared the extent to which risk factors for schizophrenia across sociodemographic, familial, neurodevelopmental, stress–adversity, emotional–behavioural and substance use domains showed different associations with PEs and depression within bivariate models that allowed for their correlation.ResultsMost of the exposures examined were associated, to a similar degree, with an increased risk of both outcomes. However, whereas female sex and family history of depression showed some discrimination as potential risk factors for depression and PEs, with stronger associations in the former, markers of abnormal neurodevelopment showed stronger associations with PEs.ConclusionsThe argument that PEs are valid markers for studying the aetiology of schizophrenia, made simply on the basis that they share risk factors in common, is not well supported. PEs seem to be a weak index of genetic and environmental risk for schizophrenia; however, studies disentangling aetiological pathways to PEs from those impacting upon co-morbid psychopathology might provide important insights into the aetiology of psychotic disorders. [ABSTRACT FROM AUTHOR]

In this study, we examined whether the proportion of tubal factor infertility (TFI) that is attributable to Chlamydia trachomatis, the population excess fraction (PEF), can be estimated from serological data using finite mixture modeling. Whole-cell inclusion immunofluorescence serum antibody titers were recorded among infertile women seen at St. Michael's Hospital in Bristol, United Kingdom, during the period 1985-1995. Women were classified as TFI cases or controls based on laparoscopic examination. Finite mixture models were used to identify the number of component titer distributions and the proportion of serum samples in each, from which estimates of PEF were derived. Four titer distributions were identified. The component at the highest titer was found only in samples from women with TFI, but there was also an excess of the second-highest titer component in TFI cases. Minimum and maximum estimates of the PEF were 28.0% (95% credible interval: 6.9, 50.0) and 46.8% (95% credible interval: 23.2, 64.1). Equivalent estimates based on the standard PEF formula from case-control studies were 0% and over 65%. Finite mixture modeling can be applied to serological data to obtain estimates of the proportion of reproductive damage attributable to C. trachomatis. Further studies using modern assays in contemporary, representative populations should be undertaken. [ABSTRACT FROM AUTHOR]